scholarly journals Synthetic Pyridoindole and Rutin Affect Upregulation of Endothelial Nitric Oxide Synthase and Heart Function in Rats Fed a High-Fat-Fructose Diet

2021 ◽  
pp. 851-863
Author(s):  
L. Salvaras ◽  
T. Kovacic ◽  
P. Janega ◽  
B. Liptak ◽  
M. Sasvariova ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Left Ventricle ◽  
Endothelial Nitric Oxide Synthase ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Control Group ◽  
High Fat ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Metabolic syndrome (MetS) belongs to the serious health complications expanding in cardiovascular diseases, obesity, insulin resistance, and hyperglycemia. In this study, hypertriacylglycerolemic rats fed a high-fat-fructose diet (HFFD) were used as an experimental model of MetS to explore the effect of tested compounds. Effects of a new prospective pyridoindole derivative coded SMe1EC2 and the natural polyphenol rutin were tested. Endothelial nitric oxide synthase (NOS3) and nuclear factor kappa B (NF-κB) expression were assessed in the left ventricle immunohistochemically and left ventricle activity was monitored in isolated perfused rat hearts. NOS3 activity in the left ventricle decreased markedly as a result of a HFFD. NOS3 expression was upregulated by both substances. NF-κB expression was increased in the MetS group in comparison to control rats and the expression further increased in the SMe1EC2 treatment. This compound significantly improved the coronary flow in comparison to the control group during reperfusion of the heart followed after ischemia. Further, it tended to increase left ventricular systolic pressure, heart product, rate of maximal contraction and relaxation, and coronary flow during baseline assessment. Moreover, the compound SMe1EC2 decreased the sensitivity of hearts to electrically induced ventricular fibrillation. Contrary to this rutin decreased coronary flow in reperfusion. Present results suggest that despite upregulation of NOS3 by both substances tested, pyridoindole SMe1EC2 rather than rutin could be suitable in treatment strategies of cardiovascular disorders in MetS-like conditions.

Using endothelial nitric oxide synthase gene polymorphisms to identify intracranial aneurysms more prone to rupture in Japanese patients

2006 ◽  
Vol 105 (5) ◽  
pp. 717-722 ◽  
Author(s):  
Boris Krischek ◽  
Hidetoshi Kasuya ◽  
Hiroyuki Akagawa ◽  
Atsushi Tajima ◽  
Akira Narita ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Intracranial Aneurysms ◽  
Tandem Repeats ◽  
Japanese Patients ◽  
Control Group ◽  
Patient Sample ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Object Recent investigators found that the presence of three tandem polymorphisms of the endothelial nitric oxide synthase (eNOS) gene—promoter single nucleotide polymorphism (SNP) T-786C, intron-4 27-bp variable number of tandem repeats, and the G894T SNP in exon 7—was indicative of intracranial aneurysms more prone to rupture in a Caucasian patient sample. In the present study, the authors sought to determine whether the presence of these eNOS polymorphisms could indicate which Japanese patients with aneurysms were more endangered by a subarachnoid hemorrhage (SAH). Methods The three eNOSpolymorphisms were genotyped in 297 patients with ruptured aneurysms (RAs), 108 patients with unruptured aneurysms (UAs), and 176 healthy volunteers by using polymerase chain reaction. The distribution of the variant alleles did not differ significantly (p > 0.05) between the RA group and the UA group. The frequency of the corresponding genotypes between the two groups and a haplotype analysis did not show any significant differences. Further comparisons of the RA and UA groups with the control group did not yield any significant allele or genotype frequency differences. Conclusions These data show that the examined set of eNOS polymorphisms were not indicative of which Japanese patients with intracranial aneurysms would suffer an SAH. The presence of eNOS polymorphisms is not useful in identifying intracranial aneurysms that are more prone to rupture in a Japanese patient sample.

Pulmonary vascular dilation induced by l‐arginine: correlation with induction of endothelial nitric oxide synthase in a rabbit model

2005 ◽  
Vol 46 (1) ◽  
pp. 48-54 ◽  
Author(s):  
S. K. Yoon ◽  
K.‐N. Lee ◽  
J. H. Lee ◽  
J. S. Jeong ◽  
J.‐Y. Kwak
Keyword(s):  
Nitric Oxide ◽  
Computed Tomography ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Tap Water ◽  
Rabbit Model ◽  
Serum Levels ◽  
Control Group ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Purpose: To determine whether oral administration of l‐arginine induces pulmonary vascular dilation, and if this pulmonary vascular dilation correlates with induction of endothelial nitric oxide synthase (eNOS) in a rabbit model. Material and Methods: Seven rabbits were fed with l‐arginine dissolved in tap water. The degree of pulmonary vascular dilation was determined using thin‐section computed tomography and the concentration of serum nitrite was measured. They were compared with four control animals. The pulmonary vascular dilation was correlated to serum levels of nitrite. Lung tissues were examined for induction of eNOS by immunohistochemistry. Results: An increased degree of pulmonary vascular dilation was found in the l‐arginine‐fed group compared to the control group ( P<0.05). Serum levels of nitrite in the l‐arginine‐fed group were higher than those in the control group ( P<0.05). Pulmonary vascular dilation correlated with serum levels of nitrite ( r2 = 0.95, P<0.05). Induction of eNOS was increased in the l‐arginine‐fed group. Conclusion: The administration of l‐arginine causes pulmonary vascular dilation, which is most likely mediated via nitric oxide through increased induction of eNOS in a rabbit model.

scholarly journals Endothelial nitric oxide synthase levels and their response to exercise in patients with slow coronary flow

2013 ◽  
Vol 24 (9) ◽  
pp. 355-359 ◽  
Author(s):  
Hakan Tasolar ◽  
Ferhat Eyyupkoca ◽  
Erdal Akturk ◽  
Yasin Karakus ◽  
Mehmet Cansel ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Coronary Flow ◽  
Slow Coronary Flow ◽  
Oxide Synthase ◽  
Response To Exercise ◽  
Endothelial Nitric Oxide

scholarly journals Mulberry Extract Attenuates Endothelial Dysfunction through the Regulation of Uncoupling Endothelial Nitric Oxide Synthase in High Fat Diet Rats

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 978 ◽  
Author(s):  
Geum-Hwa Lee ◽  
The-Hiep Hoang ◽  
Eun-Soo Jung ◽  
Su-Jin Jung ◽  
Soo-Wan Chae ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Nitric Oxide Synthase ◽  
High Fat Diet ◽  
Endothelial Nitric Oxide Synthase ◽  
High Fat ◽  
Enos Uncoupling ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Dyslipidemia is associated with endothelial dysfunction, which is linked to nitric oxide (NO) biology. The coupling of endothelial NO synthase with cofactors is a major step for NO release. This study is aimed to investigate the vascular pharmacology effects of mulberry in rat thoracic aorta and human vascular endothelial cells. In vitro, we investigated the protective effects of the mulberry extract and its main component cyanidin-3-rutinoside (C-3-R), against oxidized low-density lipoprotein (ox-LDL)-induced endothelial nitric oxide synthase (eNOS) uncoupling. Whereas ox-LDL significantly decreased NO levels in endothelial cells, mulberry extract, and C-3-R significantly recovered NO levels and phospho-eNOS Thr495 and Ser1177 expression. In vivo, mulberry was administered to 60% of high-fat diet (w/w)-fed Sprague Dawley (SD) rats for six weeks, in which endothelium-dependent relaxations were significantly improved in organ bath studies and isometric tension recordings. Consistently, aortic expressions of phospho-eNOS and nitrotyrosine were increased. Mulberry also raised serum NO levels, increased phosphorylation of eNOS, and reduced nitrotyrosine and intracellular reactive oxygen species (ROS) in aortas, showing that mulberry preserves endothelium-dependent relaxation in aortas from high-fat diet rats. We suggest that this effect is mediated through enhanced NO bioavailability, in which the regulation of ROS and its reduced eNOS uncoupling are involved.

Prevalence of common polymorphisms of AT-rich interaction domain 1A and endothelial nitric oxide synthase in patients with endometriosis compared to control group

2018 ◽  
Vol 10 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Zohreh Tavana ◽  
Azadeh Khalili ◽  
Golnaz Namazi ◽  
Ahmad Ebrahimi ◽  
Sara Davoodi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Control Group ◽  
Enos Gene ◽  
Interaction Domain ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Rich Interaction ◽  
Glu298asp Polymorphism

Introduction: Endometriosis is a common gynecologic disorder defined as ectopic presence of endometrial tissue in extrauterine sites. Endometriosis is associated with infertility and risk of malignancy. Identification of genetic factors responsible for development and malignant transformation of endometriosis can improve therapeutic approaches. In this study, we investigated the association of AT-rich interaction domain 1A ( ARID1A) and endothelial nitric oxide synthase ( eNOS) polymorphisms with endometriosis and staging of the disease. Methods: A total of 100 women with laparoscopy-confirmed diagnosis of endometriosis were included and compared with 100 women without endometriosis as the control group. Genotypes of patients regarding Gln920Ter polymorphism of ARID1A gene and Glu298Asp polymorphism of eNOS gene were determined by polymerase chain reaction techniques on blood samples from the study population. The prevalence of each genotype in endometriosis patients was compared with healthy controls using the chi-square test. Results: Significantly higher prevalence of non-CC genotype for ARID1A Gln920Ter polymorphism and non-GG genotype for G894T polymorphism of the eNOS gene was detected in the endometriosis group. There was no significant relationship between these polymorphisms and staging of endometriosis. Discussion: Significant variation of prevalence of Gln920Ter polymorphism of the ARID1A gene and Glu298Asp polymorphism of the eNOS gene among the two groups can indicate a causative effect of these genetic alterations on the development of endometriosis.

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